Worm Breeder's Gazette 16(1): 39 (October 1, 1999)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Department of Microbiology and Immunology, Stanford University Medical School, Stanford CA 94305-5124
Recent work shows that C. elegans is a useful model for pathogenesis by the bacterium Pseudomonas aeruginosa (1-4). We examined whether other pathogenic bacteria might also affect the nematode.
We exposed worms to Salmonella sp.; enteropathogenic Escherichia coli (EPEC); Listeria monocytogenes; Streptococcus bovis; Legionella sp.; Burkholderia cepacia; Mycobacterium marinum; Yersinia sp.; Shigella sp.; and Helicobacter pylori. Bacteria were grown on NGM agar where possible; the more fastidious pathogens were grown with appropriate standard media. Wild-type worms were used; for Legionella, Listeria and EPEC, we also used phm-2(ad597), which allows many bacteria to pass through the pharynx intact; aex-2(sa3), which causes constipation and thus prolongs retention of bacteria; and a phm-2; aex-2 double mutant. We observed locomotion, feeding, defecation, egg-laying, growth, and gross morphology. For every bacterial genus but one, the worms were unaffected by the pathogens and fed on them as they do on nonpathogenic E. coli.
The exception was bacteria of the genus Yersinia, which includes Y. pestis, the organism that causes plague, and the milder pathogens Y. pseudotuberculosis and Y. enterocolitica. Nematodes picked to a lawn of Y. pseudotuberculosis within hours accumulate a viscous material on their heads, which we term "nose gobs." In many animals locomotion becomes slippery: The worms bend back and forth as usual, but tend to stay in place instead of translocating across the lawn. The gobs apparently are an accumulation of Yersinia-derived material picked up as the worms move, since gobs do not appear on severely paralyzed unc-54 mutants. As nematodes remain on the lawn, they take on the pale appearance characteristic of starvation, although bacteria are plentiful and pharyngeal pumping continues. When eggs are laid on a lawn of Y. pseudotuberculosis and the parents removed, fewer than half of the larvae that hatch reach L4 stage after two days, and many animals appear starved. Similar growth inhibition also occurs, although to a lesser degree, with some strains of Y. pestis and Y. enterocolitica. Using Y. pseudotuberculosis expressing green fluorescent protein, we found no evidence that bacterial cells are entering the worm and establishing an infection.
Together, these observations suggest that Yersinia inhibits feeding by C. elegans. It is possible that the material constituting the nose gob directly plugs the mouth or pharynx. However, we cannot yet rule out a physiological, as opposed to purely physical, effect.
All pathogenic Yersinia carry a large plasmid encoding some of the organism's virulence genes. Y. pseudotuberculosis cured of its plasmid was nevertheless able to inhibit C. elegans,as was Y. pestis. We examined Y. pseudotuberculosis strains with mutations in the well-studied chromosomal virulence genes inv and ail and found that these genes also are not required to inhibit the growth of C. elegans.